Comparison of the clinical pharmacology of (-)NPA and levodopa in Parkinson's disease.
Identifieur interne : 001300 ( Istex/Corpus ); précédent : 001299; suivant : 001301Comparison of the clinical pharmacology of (-)NPA and levodopa in Parkinson's disease.
Auteurs : M Mouradian ; I Heuser ; F. Baronti ; M. Giuffra ; K. Conant ; T Davis ; T ChaseSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 1991-05.
Abstract
Direct acting dopamine agonists are generally less effective than levodopa in relieving symptoms of Parkinson's disease. In an attempt to quantitate and explain this situation, the acute motor responses to intravenous injections of the dopamine agonist, (-)-N-n-propyl-norapomorphine hydrochloride (NPA), were compared with those of the dopamine precursor, levodopa. At optimum dose levels, the acute anti-Parkinsonian efficacy of NPA averaged only about 50% of maximum, while essentially total symptom suppression was obtained with levodopa in patients previously treated with the amine precursor. Dyskinesia severity, however, was similar with the two drugs. These differences in anti-Parkinsonian efficacy may reflect the fact that while NPA acts mainly on D-2 dopamine receptors, levodopa results in stimulation of both the D-1 and D-2 subsets of receptors at a more physiological ratio. Future efforts to develop dopamine agonists for the treatment of Parkinsonian symptoms may thus have to consider focusing on drugs having pharmacological profile more similar to that of dopamine.
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DOI: 10.1136/jnnp.54.5.401
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In an attempt to quantitate and explain this situation, the acute motor responses to intravenous injections of the dopamine agonist, (-)-N-n-propyl-norapomorphine hydrochloride (NPA), were compared with those of the dopamine precursor, levodopa. At optimum dose levels, the acute anti-Parkinsonian efficacy of NPA averaged only about 50% of maximum, while essentially total symptom suppression was obtained with levodopa in patients previously treated with the amine precursor. Dyskinesia severity, however, was similar with the two drugs. These differences in anti-Parkinsonian efficacy may reflect the fact that while NPA acts mainly on D-2 dopamine receptors, levodopa results in stimulation of both the D-1 and D-2 subsets of receptors at a more physiological ratio. 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In an attempt to quantitate and explain this situation, the acute motor responses to intravenous injections of the dopamine agonist, (-)-N-n-propyl-norapomorphine hydrochloride (NPA), were compared with those of the dopamine precursor, levodopa. At optimum dose levels, the acute anti-Parkinsonian efficacy of NPA averaged only about 50% of maximum, while essentially total symptom suppression was obtained with levodopa in patients previously treated with the amine precursor. Dyskinesia severity, however, was similar with the two drugs. These differences in anti-Parkinsonian efficacy may reflect the fact that while NPA acts mainly on D-2 dopamine receptors, levodopa results in stimulation of both the D-1 and D-2 subsets of receptors at a more physiological ratio. 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In an attempt to quantitate and explain this situation, the acute motor responses to intravenous injections of the dopamine agonist, (-)-N-n-propyl-norapomorphine hydrochloride (NPA), were compared with those of the dopamine precursor, levodopa. At optimum dose levels, the acute anti-Parkinsonian efficacy of NPA averaged only about 50% of maximum, while essentially total symptom suppression was obtained with levodopa in patients previously treated with the amine precursor. Dyskinesia severity, however, was similar with the two drugs. These differences in anti-Parkinsonian efficacy may reflect the fact that while NPA acts mainly on D-2 dopamine receptors, levodopa results in stimulation of both the D-1 and D-2 subsets of receptors at a more physiological ratio. Future efforts to develop dopamine agonists for the treatment of Parkinsonian symptoms may thus have to consider focusing on drugs having pharmacological profile more similar to that of dopamine.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Comparison of the clinical pharmacology of (-)NPA and levodopa in Parkinson's disease.</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Comparison of the clinical pharmacology of (-)NPA and levodopa in Parkinson's disease.</title></titleInfo><name type="personal"><namePart type="given">M M</namePart><namePart type="family">Mouradian</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I J</namePart><namePart type="family">Heuser</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Baronti</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Giuffra</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Conant</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T L</namePart><namePart type="family">Davis</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T N</namePart><namePart type="family">Chase</namePart><affiliation>Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article">research-article</genre><subject><genre>heading</genre><topic>Research Article</topic></subject><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">1991-05</dateIssued><dateCreated encoding="w3cdtf">1991-05-01</dateCreated></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Direct acting dopamine agonists are generally less effective than levodopa in relieving symptoms of Parkinson's disease. In an attempt to quantitate and explain this situation, the acute motor responses to intravenous injections of the dopamine agonist, (-)-N-n-propyl-norapomorphine hydrochloride (NPA), were compared with those of the dopamine precursor, levodopa. At optimum dose levels, the acute anti-Parkinsonian efficacy of NPA averaged only about 50% of maximum, while essentially total symptom suppression was obtained with levodopa in patients previously treated with the amine precursor. Dyskinesia severity, however, was similar with the two drugs. These differences in anti-Parkinsonian efficacy may reflect the fact that while NPA acts mainly on D-2 dopamine receptors, levodopa results in stimulation of both the D-1 and D-2 subsets of receptors at a more physiological ratio. Future efforts to develop dopamine agonists for the treatment of Parkinsonian symptoms may thus have to consider focusing on drugs having pharmacological profile more similar to that of dopamine.</abstract><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="JournalID-hwp">jnnp</identifier><identifier type="JournalID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>1991</date><detail type="volume"><caption>vol.</caption><number>54</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>401</start></extent></part></relatedItem><identifier type="istex">78FD56098F13A2E7E676D3043F36C25802A5F1B1</identifier><identifier type="DOI">10.1136/jnnp.54.5.401</identifier><identifier type="href">jnnp-54-401.pdf</identifier><identifier type="PMID">1865201</identifier><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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|clé= ISTEX:78FD56098F13A2E7E676D3043F36C25802A5F1B1
|texte= Comparison of the clinical pharmacology of (-)NPA and levodopa in Parkinson's disease.
}}
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